There are a variety of mechanical signals in the microenvironment of cells, which have temporal and spatial variability, which jointly regulate the histological processes such as cell proliferation, differentiation and migration. Piezo1 is a mechanically sensitive cationic channel. As a force sensor, it transmits signals to downstream pathways and participates in a variety of life activities in response to changes in the cell microenvironment. In this paper, the common signal pathways of Piezo1 were reviewed in order to identify the downstream signaling pathways regulated by Piezo1, thereby providing theoretical basis for inhibiting or delaying related diseases.

 Tumor is the main lethal type of major diseases that human beings are facing nowadays. Traditional therapies, such as chemotherapy, surgery, radiotherapy, etc, have been the mainstay of tumor treatment for a long time, and still have their own limitations in terms of effectiveness. In recent years, immunotherapy for tumors has attracted much attention with the rise of strategies such as immune checkpoint inhibitors, chimeric antigen receptor T-cell (CAR-T) relay therapy, and anti-tumor vaccines. Among them, CAR-T cell therapy, as a breakthrough tumor immunotherapy method, can precisely target tumors at the cellular and molecular levels by modifying the patient’s own T cells to express recombinant antigen receptors targeting specific tumor antigens, breaking the restriction of the major histocompatibility complex (MHC) of the natural T cells themselves. It can precisely target tumors at the cellular and molecular levels, and thus can efficiently and specifically identify and kill cancer cells, providing a new perspective for treatment. Since the approval of the first CAR-T therapy by the US Food and Drug Administration (FDA) in 2017, in addition to still maintaining significant advantages in the field of classical multiple hematologic malignancies, it has also made outstanding progress in the treatment and clinical trials of some solid tumors and autoimmune diseases, among others. This paper  will briefly review the current principles, applications, challenges and directions of development of CAR-T technology. 

Objective To investigate the antitumor effects of triptolide against CT26 colon cancer and its impact on the expression of Polo-like kinase-1 (PLK-1) protein.  Methods  Forty clean grade BALB/c mice, each mouse was implanted with 1×10⁶ CT26 cells into the dorsal side of the right forelimb to establish a tumor-bearing mouse model. Experimental animals were randomly divided into four groups, the tumor model group (saline control), the positive drug group ［oxaliplatin, 5mg/(kg·d)］, the low-dose triptolide group ［50μg/(kg·/d)］, and the high-dose triptolide group ［100μg/(kg·d)］. The drugs were administered through intraperitoneal injection (10 times in total, once every other day). The in vitro effects of the drugs on the proliferation, migration, invasion, and mitosis of CT26 cells were also assessed.   Results  Triptolide significantly inhibited the proliferation, migration, and invasion of CT26 colon cancer cells, and disrupted the separation of centrosomes and the correct arrangement of chromosomes during the prophase of mitosis in tumor cells. The binding energy of triptolide and PLK-1 protein was -7.1 kcal/mol, and it could down-regulate the expression of PLK-1 in CT26 cells.  Conclusion  Triptolide exerts its antitumor effects against CT26 colon cancer by downregulating the expression of PLK-1.

Objective To explore the mechanism of action of jolkinolide B in the treatment of gastric cancer by network pharmacology combined with molecular docking technique.   Methods The SwissTargetPrediction database was used to obtain the targets of the active compounds. Search Genecards, OMIM, Drugbank, TTD, and PharmGKB databases to obtain targets for gastric cancer. The intersection between the targets of jolkinolide B and those of gastric cancer was identified pinpoint potential targets for jolkinolide B in treating gastric cancer. The String database was utilized construct a protein-protein interaction(PPI) network. Bioconductor bioinformatics packages with R software was employed conduct Gene Ontology (GO) functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis on the shared targets. This process revealed significant regulatory pathways crucial for jolkinolide B’s efficacy in treating gastric cancer. Cytoscape 3.7.1 software was utilized create the core network of “Potential Targets of Triptolide B in Gastric Cancer Treatment”, and SYBYL-X2.1.1 software was employed conduct molecular docking validation of the selected main active ingredients and critical targets.   Results Jolkinolide B may target multiple proteins, including MAPK1, glycogen synthase kinae-3β(GSK-3β), and JUN, impacting the proliferation, invasion, and metastasis of gastric cancer, ultimately inhibiting its growth.     ConclusionWe predicted the possible molecular mechanism of jolkinolide B in the treatment of gastric cancer to provide guide information for the subsequent experimental research and clinical application.

Objective To explore whether creatine therapy regulates neuronal ferroptosis by inhibiting the activation of STAT1 signaling pathway associated with suppressor of cytokine signaling 1 (SOCS1) in Alzheimer’s disease.   Methods  Immunohistochemical staining and counting of positive results using paraffin sections of human brain frontal lobes were employed to determine the trend of changes in the target proteins. Further validation was performed by immunofluorescence and Western blotting. STAT1 phosphorylation was inhibited by creatine injection using eleven FAD4Tmice and by cerebellar medullary pool puncture, and the expression of target proteins was examined by immunohistochemistry and immunofluorescence after postmortem sampling.   Results  Compared with the age controls, interferon-γ (IFN-γ), an activating cytokine of the STAT1 signaling pathway, and SOCS1, a negative regulator of STAT1 activation, were both significantly up-regulated, STAT1 phosphorylation was enhanced, and the ferroptosis markers ferritin light chain (FTL) and cystine/glutamate transporter(xCT) increased markedly in the cortex of AD human brains; Creatine treatment of FAD4Tmice resulted in a reduction of both IFN-γ and SOCS1, and a significant decrease in the ferroptosis markers FTL and xCT (SLC7A11).  Conclusion  Creatine ameliorates neuronal ferroptosis in AD model mice by reducing neuronal STAT1SOCS1 signalling activation. 

  浙江大学和中国医学科学院北京协和医学院先后于2012年启动了人脑库建设工作，推动了我国人脑库建设的发展。2014年，“中国人脑组织库建设国际研讨会”在长沙和北京两地成功举办，这次研讨会标志着中国人脑库联盟的初步形成，也意味着我国脑库工作开始正式且系统地展开。此后，我国人脑样本的收集数量显著增加，脑库的建设和管理也日益规范化、专业化［5］。为了进一步促进交流与合作，我国在2014年、2016年、2018年和2022年连续举办了四届“中国人脑组织库建设研讨会”。特别是在2016年，中国人脑组织库协作联盟正式成立，这一联盟为我国各人脑库提供了一个共同交流和协作的平台。随着我国“脑计划”的深入推进，联盟成员已由最初的10家医学院校扩展至现今的27家成员单位，共同助力中国人脑组织库的发展壮大［2］。 

    近年来，随着我国“脑计划”的展开，人脑库的建设也逐渐加速。然而，与国内庞大的科研需求相比，人脑组织库的规模和质量仍有待提升。在人脑组织库的建设中，脑组织的收集数量固然重要，但更为核心的是确保脑组织的质量。高质量的脑组织样本是神经科学研究得以深入进行的基石，它直接关系到研究成果的可靠性和有效性。中国人脑组织库标准化操作方案（standardized operating protocols, SOP）是人脑库建设的重要成果之一，它规范了人脑组织样本的收集、处理、保存和共享的各个环节，确保样本的可靠性和一致性。截至目前，为了满足神经科学领域不断发展的需求，中国人脑组织库协作联盟已经成功制定SOP（2017版）［6，7］并更新（2022版）［8］，同时还推出了一版脊髓取材SOP［9］，以适应神经科学领域的发展需求。中国人脑组织库协作联盟定期开展培训和交流活动，确保各成员单位能够熟练掌握SOP并正确应用于实际工作中。27家脑库联盟成员单位以国家发育和功能人脑组织资源库（中国医学科学院基础医学研究所）、国家健康和疾病人脑组织资源库（浙江大学）、中南大学湘雅医学院人脑组织库和复旦大学上海医学院人脑组织库为核心单位，成立了覆盖全国的人脑组织库协作共建网络，各成员单位及研究人员在人脑组织样本的收集、共享与应用方面做出了重要贡献［10，11］。以河北医科大学人脑组织库为例，该脑库是最早一批加入“中国人脑组织库协作联盟”的单位之一，自2019年成为国家发育和功能人脑组织资源库共建单位以来，已收集保存人脑样本30例，并按照中国人脑组织库标准化操作方案进行了取材、整理及测定等相关工作。 

  河北医科大学人脑组织库2019年12月~2024年2月间收集的30例捐献者样本进行了深入分析和总结，所有工作均严格遵循中国人脑组织库标准化操作方案的指导原则。首先，河北医科大学人脑组织库在样本收集方面展现了高效的组织管理与执行能力。通过对收集样本的统计分析，我们可以看到捐献者的基本信息，如性别、年龄和死亡原因等，这为后续的科学研究提供了重要的参考依据。其次，死亡后取材延误时间较短，12 h 以内的样本占 90%，保证了样本的新鲜度和研究价值。同时，样本的RNA完整性较好，脑脊液pH值稳定，这为后续的分子生物学和病理学研究提供了坚实的基础。 

  在建设过程中，河北医科大学人脑组织库特别强化了病理评估和诊断环节，这是确保人脑样本质量与研究可靠性的核心要素。为了提升病理评估的准确性，河北医科大学人脑组织库派遣工作人员前往荷兰脑库访问，学习并引进其先进的病理诊断技术，现已经建立了11种病理诊断染色技术（如基础染色 HE，特殊染色 Gallyas、Bielschoesky、Congo Red组织学染色，Aβ、p-tau、p-TDP43免疫组织化学染色等），并且能准确诊断多种脑病理疾病（包括阿尔茨海默病、帕金森病、多系统萎缩和皮质基底节变性等）。为了进一步促进国内外脑库与研究机构之间的合作与交流，河北医科大学人脑组织库在2023年成功承办了“第1期人脑组织库样本神经病理诊断阅片培训班”，通过共享数据、技术和经验交流，不断提升病理评估和诊断水平，同时也为人脑科学研究领域做出了积极贡献。 

    随着我国“脑计划”的深入推进，人脑库在国内神经科学研究领域的重要性日益凸显。通过标准化操作和对病理评估与诊断的不断强化，我国人脑组织库正努力提供高质量的研究样本，助力科学家们深入探索大脑的奥秘，这不仅体现了我国在科研领域的实力和决心，也展示了对人类健康与疾病研究的高度重视。我们期待，随着我国人脑库的持续发展和完善，其将为世界神经科学研究贡献更多中国智慧和中国方案，进一步推动人类对大脑和神经系统的认知，为神经系统疾病的预防和治疗提供更有效的策略。

Objective To develop a melanoma diagnosis framework based on large-scale vision-language models, and to explore the feasibility and accuracy of the framework for melanoma diagnosis.   Methods The publicly available Derm7pt dataset, which was divided into a training set (346 cases), a validation set (161 cases), and a test set (320 cases) was utilized. A melanoma diagnosis framework based on large-scale vision-language models was proposed, comprising two text branches and one visual branch. In the text branches, one branch processed fixed clinical prompts, while the other handled learnable prompts. This design aimed to optimize the effectiveness of learnable prompts through guidance from fixed clinical prompts. The visual branch processed dermoscopic images and enhanced melanoma feature recognition through fine-tuning the image encoder.   Results On the Derm7pt dataset, our method  outperformd other existing method. It achieved an area under the receiver operating characteristic curve (AUC) of 87.35%, an accuracy of 84.17%, and an F1-score of 84.01%.   Conclusion The study demonstrates that with appropriate fine-tuning strategies, methods based on large-scale vision-language pre-trained models can effectively adapt to melanoma diagnosis tasks. This approach can serve as a powerful auxiliary tool for doctors, helping them make more accurate diagnostic decisions.

Objective  To construct a three-dimensional statistical shape model of the pelvis and analyze the individual variation and gender differences of the three-dimensional shape of the pelvis. Methods  We collected CT data from 201 Chinese individuals and used deep learning to automatically reconstruct three-dimensional models of the pelvis. Through three-dimensional model registration, dense correspondence mesh mapping, and the use of statistical shape modelling (SSM) and principal component (PC) analysis method, we extracted models of variations (MoV) of pelvic shape changes and statistically compared the shape MoV between males and females. Results  We analysed the top 10 principal components of shape variations, which accounted for 86.1% of the total variability. Among them, PC01, PC02, and PC04 showed significant differences between genders (P <0.001), accounting for a total variability of 60.1%. PC08 and PC10 demonstrated pelvic asymmetry, accounting for a total variability of 3.8%. Conclusion  We constructed a three-dimensional statistical shape model of the pelvis in Chinese individuals, revealing the morphological variation and sex differences of Chinese pelvis.  

Objective To  explore the mechanism of cinobufagin (CBG) in treating gastric cancer based on network pharmacology combined with bioinformatics and molecular docking technology.   Methods Active ingredients and potential targets of CBG in treating gastric cancer were collected from PubChem, TCMSP, and SwissTargetPrediction databases. Transcriptional data of gastric cancer samples were obtained from TGGA database, and gastric cancer-related targets were identified through differential gene analysis. Intersection of targets between CBG and gastric cancer diseases was subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. Protein-protein interaction (PPI) network of common targets was constructed using STRING database, and core targets were selected using Cytoscape software. Molecular docking verification of core targets screened with SYBYL-X 2.1.1 software was conducted with CBG.       Results CBG treatment of gastric cancer involved 59 targets, with 19 key targets identified. Key targets such as aurora kinase A(AURKA), cyclin-dependent kinase 1(CDK1), enhancer of zeste homolog 2(EZH2), hepatocyte growth factor receptor (MET), matrix metallopeptidase 3(MMP-3), progesterone receptor (PGR), prostaglandin-endoperoxide synthase 1(PTGS1), and thymidylate synthase (TYMS) which exhibited good binding activity with CBG and were closely associated with gastric cancer prognosis.    Conclusion CBG may exert anti-gastric cancer effects through multiple targets and pathways.

Objective  To explore the effect of gastrodin（GAS）on the polarization of M2 microglia under oxygen and glucose deprivation（OGD）and the effect of p38 MAPK inhibition on the polarization status of microglia.  Methods BV2 microglia was divided into the control group（Ctrl），p38 MAPK inhibitor SB203580 group（I），OGD group (OGD)，OGD+I group，gastrodin treatment group（G+OGD），and G+OGD+I group. The expressions of p38 MAPK，phosphorylated p38 MAPK（p-p38 MAPK）, M2 microglia marker arginase-1 (Arg-1) and chitinase like protein 1/2（YM1/2）were detected by immunofluorescent staining and Western blotting. Results  Immunofluorescent staining results showed that the pretreatment with gastrodin reduced the fluorescence expression of p-p38 MAPK in OGD induced BV2 microglia, enhanced the fluorescence expressions of Arg-1 and YM1/2. After pretreatment with SB203580，the fluorescence expressions of p-p38 MAPK further decreased，the fluorescence expressions of Arg1 and YM1/2 further increased，both were significantly different from the G+OGD group （ n=3，P<0.05）. The fluorescence expressions of p38 MAPK in each group was not statistically significant（ n=3，P>0.05）. Western blotting results showed that the protein expressions of p-p38 MAPK, Arg-1 and YM1/2 in the OGD group enhanced，compared with that in the control group（ n=3，P<0.05）. After the pretreatment with gastrodin，the protein expression of p-p38 MAPK was reduced significantly，the protein expressions of Arg-1 and YM1/2 was enhanced obviously，both were significantly different from the OGD group （ n=3，P<0.05）. After pretreatment with SB203580，the protein expressions of p-p38 MAPK was further reduced，the protein expression of Arg-1 and YM1/2 were further enhanced，both were significantly different from the G+OGD group（ n=3，P<0.05）. In addition，there was no significant change in p38 MAPK protein expression among groups （ n=3，P>0.05）.  Conclusion  Gastrodin inhibits p38 MAPK signaling activation to promote BV2 microglial polarization towards the M2 phenotype，reducing inflammatory responses and exerting a protective effect. 

Objective To investigate the differentiation of oligodendrocyte precursor cells after neural injury utilizing Sox10 cell lineage tracing in the cortical tissue. Methods  C57BL/6 mice and Sox10-CreERT2/red fluorescent protein(RFP) model mice were used in the current study. The Sox10-CreERT2/RFP model mice generated by crossing Sox10-CreERT2 and Ai9 were 8-week-old F1 mice (n =16), which were randomly divided into control group (n =4) and 7 days (n =4), 14 days (n =4), and 30 days feed groups (n =4). Tamoxifen(TAM) was used to induce the expression of RFP. The control group received tamoxifen dissolved in sunflower seed oil by gavage (40 mg/kg once daily for three consecutive days) and the brain tissues were obtained after 4 days. The feed group mice were fed with tamoxifen-containing feed to induce RFP expression, and the brain tissues were obtained after 7, 14, and 30 days, respectively. Immunofluorescent staining was performed to detect the expressions of neuronal nuclei (NeuN), microtubuleassociated protein 2 (MAP2), phosphorylated histone 2AX (γ-H2AX), cluster of differentiation 13 (CD13), γaminobutyric acid (GABA), glial fibrillary acidic protein (GFAP), cluster of differentiation 11b (CD11b), vesicular glutamate transporter 2 (VGLUT2), and adenomatous polyposis coli (APC, CC-1) in the brains of each group mice. The number of positive cells was counted, and the proportion was calculated. Eight-week-old male C57BL/6 mice were randomly divided into wild type(WT) group (n =4) and WT+TAM group (n =4). They were fed with regular feed and tamoxifencontaining feed for 30 days, respectively, and then brain tissues were obtained. Immunofluorescent double-labeling was used to detect the expressions of γ-H2AX positive neurons in the cortex of mice in both groups.   Results  In the control group, feed 7 days,14 days, and 30 days groups, the proportions of RFP⁺ pericytes among all RFP⁺ cells in the cortical tissue were (0.8±0.1)%, (2.7±0.1)%, (3.2±0.1)%, (4.0 ±0.1)%, respectively, and the proportion of mature oligodendrocytes (CC-1⁺ RFP⁺) in the feed 7 days group was (51.2±0.7)%. The proportions of RFPpositive neurons in the cortex after 14 and 30 days of tamoxifen feed were (0.7±0.1)% and (1.5±0.1)%, respectively, while no conversion to RFP-positive neurons was observed in the gavage group and 7 days feed group. RFP cells in the cortex of the 7 days or 30 days feed group did not express GFAP or CD11b. Extensive γ-H2AX⁺ NeuN⁺ staining was observed in the WT group and WT+TAM group. Conclusion  Long-term administration of tamoxifen can promote the differentiation of Sox10 cells into pericytes and neurons. Further investigation into the role of OPC in the neurovascular unit repair mechanism may contribute to a better understanding of the pathogenesis underlying AD. 

Objective To observe the difference of bone micro-structure in different regions of proximal femur, micro-CT scanning was performed on 30 proximal femur specimens to explain the mechanism of proximal femur fracture and to provide anatomical basis for prosthesis design.     Methods Totally 30 intact proximal femur specimens were obtained from 60-80 year-old cadavers. Micro-CT scanning was used to measure the trabecular thickness(Tb.Th), trabecular number(Tb.N), trabecular space(Tb.Sp), connectivity(Conn) and bone mineral density(BMD) and other parameters in 7 regions of proximal femur, including proximal pressure trabecular(PPT), distal pressure trabecular(DPT), femoral head-neck junction(FHNJ), head and neck of femoral neck(HNFN), the base of femoral neck(BPFN), intertrochanteric line(IL) and greater trochanter(GT).    Results The bone mineral density of IL and GT were higher than those of BPFN, FHNJ, DPT and PPT. The trabecular thickness of GT was the largest, followed by IL, BPFN and HNFN, and the smallest was FHNJ, DPT and PPT. The trabecular space of IL was larger than that of GT, and the data of both were larger than those of other parts, among which DPT and PPT were the smallest. The trabecular number of IL and GT were the smallest, BPFN, HNFN and FHNJ were larger, and DPT was the largest. The volume fraction of IL was the smallest, BPFN and HNFN were larger, DPT and PPT were the largest.     Conclusion The bone density, trabecular thickness, bone volume, and total volume of GT and IL in the proximal femur of elderly patients are all relatively large, so the reason for the high incidence of fractures is not due to weak internal bone microstructure; The bone density, trabecular thickness, and trabecular gap at the proximal and distal ends of the vertical trabecular bone are relatively small. If it is necessary to perform core decompression for prosthesis filling at this location, the design should be conducive to the mechanical conduction of the prosthesis and the regeneration of surrounding bone tissue.

 Human brain banks use a standardized protocol to collect, process and store post-mortem human brains and related tissues, along with relevant clinical information, and to provide the tissue samples and data as a resource to foster neuroscience research according to a standardized operating protocols (SOP). Human brain bank serves as the foundation for neuroscience research and the diagnosis of neurological disorders, highlighting the crucial rule of ensuring the consistency of standardized quality for brain tissue samples. The first version of SOP in 2017 was published by the China Human Brain Bank Consortium. As members increases from different regions in China, a revised SOP was drafted by experts from the China Human Brain Bank Consortium to meet the growing demands for neuroscience research. The revised SOP places a strong emphasis on ethical standards, incorporates neuropathological evaluation of brain regions, and provides clarity on spinal cord sampling and pathological assessment. Notable enhancements in this updated version of the SOP include reinforced ethical guidelines, inclusion of matching controls in recruitment, and expansion of brain regions to be sampled for neuropathological evaluation.

Objective To investigate the related mechanism which metformin inhibited the proliferation of HCT116 colorectal cancer cells via down-regulating the expression of up-frameshift protein 1 (UPF1).     Methods TCGA and UALCAN databases were utilized to analyze the expression level of UPF1, while Western blotting and Real-time PCR were performed to validate the differences of UPF1 expressions in colon cancer tissues and adjacent normal tissues. Clone formation assay, CCK-8 assay, wound healing assay and Transwell invasion assay were used to examine the effects of knockdown UPF1 on the proliferation, migration and invasion of HCT116 cells respectively. The HCT116 cell dataset with UPF1 knockdown was screened from GEO database for Kyoto Encydopedia of Genes and Genomes(KEGG) pathway analysis, the expression level of differential genes that enriched in Hippo pathway were verified by Real-time PCR. The HCT116 cells were treated with metformin, Western blotting and Real-time PCR were employed to detect the UPF1 expression. Mendelian randomization analysis was performed to explore the causal association between metformin treatment and colorectal cancer.     Results Analysis of TCGA and UALCAN databases showed that both UPF1 mRNA and protein were highly expressed in colon cancer tissues and the expression level of UPF1 was closely correlated with clinicopathologic stage and lymph node metastasis. Compared with adjacent normal tissues, the UPF1 protein and mRNA were highly expressed in colon cancer tissues. Knockdown UPF1 expression could inhibit the proliferation, migration and invasive ability of HCT116 cells. There were 8 differential genes affect the Hippo pathway by KEGG enrichment analysis, Real-time PCR experiments confirmed that CTNNB1, BMP4, TEAD2, PARD6G and FZD1 mRNA decreased in HCT116 cells with UPF1 knockdown. Both UPF1 protein and mRNA expressions decreased after metformin treatment in HCT116 cells. Mendelian randomization analysis showed a negative causal association between metformin treatment and colorectal cancer.      Conclusion Knockdown of UPF1 expression inhibits the proliferation of HCT116 cells through regulating Hippo pathway. Metformin can reduce the UPF1 expression for further inhibiting the proliferation of colorectal cancer cells.

 Glioblastoma multiforme (GBM) is the most common primary malignant brain tumor of the central nervous system in adults, with a median survival of less than 15 months. The tumor microenvironment (TME) of GBM includes extracellular matrix and a variety of immune cells, including tumor-associated macrophages, microglia and myeloid-derived suppressor cells. The interaction between these cells and tumor cells plays a key role in the occurrence and development of GBM. The heterogeneity of GBM microenvironment is one of the main reasons for the poor efficacy of many therapies. Therefore, understanding the interaction between GBM and its tumor microenvironment is helpful to explore new targeted therapeutic strategies, which is expected to provide better treatment options for patients, thereby improving patient prognosis.

Objective  To investigate the spatiotemporal variations in sexual size dimorphism among Chinese Han students.  Methods  Based on the eight students’physical and healthy investigations, the data on the stature and body mass were systematically collected for 343 928 and 344 029 Chinese Han students aged 19 to 22 years from 1985 to 2019, respectively. The sexual stature dimorphism index (SSDI) and sexual body mass dimorphism index (SBMDI) were employed to analyze the distribution in different periods and regions. In addition, we focused the relationships between these two indices and the per capita consumption expenditure. Results  Positive secular trends were observed in the SSDI and SBWDI among Chinese Han students throughout the 1985 to 2019 period. Notable similarities were identified in the SSDI and SBWDI between northern and southern students. Compared with the SSDI, the SBWDI exhibited significant disparities between urban and rural areas, and demonstrated a positive association with the per capita consumption expenditure.  Conclusion  The female buffering hypothesis possesses a limited range of spatiotemporal adaptability, and the trait more susceptible to environmental influences is better suited to test this hypothesis. 

Objective To identify differentially expressed genes (DEGs) during the early stage of differentiation of human embryonic stem cells (hESCs) into insulin-producing cells (IPCs) and construct the microRNA(miRNA)-mRNA regulatory network.   Methods The datasets GSE42094 from Gene Expression Omnibus (GEO) were employed in this study and included hESCs, Diff1, Diff2, Diff3, Diff4 and IPCs groups. DEGs in the Diff1 group were selected and gene ontology(GO) and Keyoto Encyclopedia of Genes and Genomes(KEGG) pathway were deciphered. The miRNAs associated with DEGs were predicted and the miRNAmRNA regulatory network was visualized. Then the predicted miRNA was validated by paper result.   Results GO result  demonstrated that the significant term of biological process were “cell migration involved in gastrulation” and “SMAD protein signal transduction”. The KEGG pathway analysis indicated that “transformating growth factor(TGF)-beta signaling pathway” and “Signaling pathways regulating pluripotency of stem cells” played essential roles for 28 DEGs in the Diff1 group. To predict miRNA associated with DEGs, we found that miR-335-5p may regulate expressions of CDA, IFITM1, FREM1, FGF17 and ROR2 genes. There were 26 miRNAs which were validated by result  of paper.    Conclusion The miRNA-mRNA regulatory network plays an essential role during the early stage of the induction of IPCs. 

 Integrins are transmembrane receptors that can coordinate signal transduction between cells and extracellular matrix or between cells. The abnormal function of integrins is one of the recognized mechanisms of tumor development. As an important regulatory mode, post-translational modification can change the conformation and physicochemical properties of proteins, thus affecting their activities, stability and functions. After the modification of the integrin, such as glycosylation and methylation, the corresponding signal transduction pathway changes, and then affects cell adhesion, migration, differentiation and other life activities, involving in diverse physiology and pathological processes. Post-translational modifications of integrins are abundant in tumor progression and play a key role in regulating the growth, metastasis and drug resistance of different tumor cells. In this review, the structure and function, post-translational modification of integrins, and their relationship with occurrence and development of tumors will be discussed, in order to provide more explorable targets for the treatment of cancer.

Objective  To investigate the infiltration of peripheral monocyte in the hippocampal CA3 area in neuralgia mice at different time points and explore the effects of the infiltration on neuralgia and the neuralgia-induced anxiety-like behavior in mice. Methods  The healthy male C57 mice were randomly divided into four groups: sham, sciatic nerve branch selective injury（SNI）model （SNI）, CCR2 inhibitor RS102895 (SNI + RS102895) and microglial inhibitor minocycline (MC) (SNI + MC) groups. Both the sham and SNI groups were further divided into 7 days, 14 days and 18 days groups, and the SNI + RS102895 and SNI + MC groups were sampled on the 18th day. Neuralgia was induced by SNI, and mechanical hyperalgesia was assessed by paw withdrawal threshold (PWTs) at different time points. Elevated plus maze (EPM) and open field test (OFT) were performed respectively two days and one day before sacrifice. Immunofluorescence was used to observe the expressions of leukocyte differentiation antigen 45 (CD45) and the co-expression with microglial markers ionized calcium binding adaptor molecule-1(IBA-1), transmembrane protein 119 (TMEM119), astrocyte marker glial fibrillary acidic protein (GFAP), and neuronal marker neuronal nuclei (NeuN) in the hippocampal CA3. The percentage of monocytes in the whole brain of 14 days SNI mice was determined by flow cytometry. Minocycline at 90 mg/(kg·d),  RS102895 at 5 mg/(kg·d) and saline were administered orally on the 5th to 16th day in the corresponding 18 days groups, and the effects of blocking monocyte infiltration on neuralgia and anxiety-like behavior and the expressions of CD45 and IBA-1 in CA3 region of hippocampus were observed.  Results  On the first day after SNI, the PWTs of mice in the 7 days and 14 days groups decreased and continued until before sacrifice( P< 0.01). The CD45 expression did little in the 7 days sham group. Compared with the sham group at the same time point, the CD45 expression did not increase in 7 days SNI mice (P>0.05) and increased significantly in 14 days SNI mice ( P <0.01), only slightly co-expressed with IBA-1 and TMEM119 and no co-expression with GFAP and NeuN, the percentage of monocytes in the whole brain increased significantly in 14 days SNI mice ( P<0.01). Inhibition of microglial activation or CCR2 expression reduced the expression of CD45 in the CA3 in SNI mice (P <0.01), increased the PWTs ( P <0.01) and alleviated anxiety-like behavior in SNI mice (P<0.01).  Conclusion  There was an infiltration of peripheral monocytes in the hippocampal CA3 region after 14 days of SNI-induced neuralgia, which might be involved in the maintenance of neuralgia and the development of neuralgia-induced anxiety-like behaviors. 

Objective To initially explore the possibility of applying the fluorescence micro-optical sectioning tomography (fMOST) high-resolution 3D reconstruction system to the morphological study of the intestinal nervous system and to preliminarily establish a method  for studying the morphology of the intestinal nervous system using this system.    Methods fMOST high-resolution 3D reconstruction system was used to study the intestinal nervous system of C57BL/6 mice in detail. Based on this method, a new morphological method  of the visceral nervous system of small animal models was explored at the single-cell level.   Results Compared with the large intestine, the small intestine lacked the typical myenteric plexus (Auerbach), deep mucosal plexus (Henley), and submucosal superficial plexus (Meissner).   Conclusion The result  of this paper provide a clearer and systematic display of the anatomical structure of the enteric nervous system in C57BL/6 mice, and further clarify the similarities and differences between the enteric nervous system of mice and human, and provide a theoretical basis for its rational application in the study of digestive system diseases. The morphological study of fMOST high-resolution 3D reconstruction system is not limited to the central nervous system, but can be extended to the morphological study of multiple visceral nervous systems.

Objective To propose a high-precision deep learning-based image assessment method  of osteosarcoma chemotherapy efficacy for clinical treatment, as existing methos have low accuracy of osteosarcoma assessment.   Methods The low incidence of osteosarcoma led to the small scale of its imaging data and the problem of imbalance in data categories. This study combined deep learning with clinical medical information, combined the bone sarcoma generation module of BoneGAN and the scale lesion information capture module, and proposed OMLA-Net, a deep learning assessment network for chemotherapy effect of bone sarcoma based on multi-scale lesion attention network, which achieved computer-aided bone tumor assessment with integrated data augmentation and focused lesion information through pre-training and generalized loss training. Results  In this study, 40 cases of osteosarcoma MRI data were used as the basis for the comparison test on the generated dataset, and the OMLA-Net assessment outperformed the SOTA method  Conv-LSTM-GAN in terms of the assessment effects such as accuracy and F1 scores, and the difference was statistically significant (P<0.05); the subsequent K-fold cross-validation ablation experiments further demonstrated the effectiveness of each module proposed by OMLA-Net.   Conclusion   OMLA-Net can effectively perform the impact assessment of chemotherapy effect on osteosarcoma, which provides a new idea for subsequent clinical application.

Objective  To explore an experimental protocol for differentiating humaninduced pluripotent stem cells (iPSCs) into highly pure midbrain dopaminergic (DA) neurons.    Methods  By optimizing a blend of small molecules and recombinant human growth factors, iPSCs were induced to differentiate into ventral midbrain floor plate DA progenitor cells and subsequently into mature substantia nigra pars compacta DA neurons. Throughout the differentiation process, Real-time PCR and immunofluorescent staining were utilized as a method  for quality assessment. Results  iPSCs firstly differentiate into dopaminergic precursor cells, and then gradually differentiate into DA neurons expressing tyrosine hydroxylase (TH).     Conclusion  The protocol successfully yields approximately high purity tyrosine hydroxylase-positive (TH+) DA neurons. This differentiation technique offers an effective cellular model for studying the physiological mechanisms and pathogenesis of Parkinson’s disease, providing valuable insights for future research and potential therapeutic strategies. 

Homeobox(HOX) genes encode a group of proteins that are highly conserved and closely related to the axial differentiation of embryos. The disorder of segmental development caused by HOX genes deficiency or abnormal expression has been observed in drosophila and mice. However, subsequent studies have found that proteins encoded by the HOX gene family are also involved in the regulation of tumor genesis and development. The roles of the whole HOX family had been reviewed by the author in the past, and through the in-depth researches, the author paid attention to the pivotal role of HOXB9 and made new progress in the study of post-translational modifications of this protein. Taking HOXB9 as a clue, this review summarizes the tumor-related signaling pathways and the modulating effects of post-translational modification of HOXB9 on tumor progression, as well as the possible research directions in the future.

Objective  To investigate the activated phenotype and the expression of the receptor of advanced glycation endproducts (RAGE) of astrocytes after hypoxicischemic brain damage(HIBD) in neonatal rats and the effects of gastrodin (GAS) intervention on them. Methods Totally 48 neonatal 3 days SD rats were used to construct HIBD model and randomly divided into sham group, HIBD group and HIBD+GAS group(100 mg/kg), and the expressions of A1 type astrocyte marker C3, A2 type astrocyte marker S100A10, RAGE, tumor necrosis factor-α (TNF-α), brain-derived neurotrophic factor(BDNF), and insulin-like growth factor(IGF-1) in the corpus callosum of the ischemic side were detected by Western blotting and immunohistochemical staining on day 1 and day 3 after HIBD.TNC-1 cells were divided into control group, oxygen glucose deprivation(OGD) group, OGD+GAS (0.34mmol/L) group and GAS group, and then the protein expressions of RAGE, TNF-α, BDNF and IGF-1 were detected by Western blotting and immunofluorescence. Results  In vivo, Western blotting showed that compared with the sham group, the protein expression levels of C3, S100A10, RAGE, TNF-α and IGF-1 in the 1 day and 3 days groups after HIBD group in 1 day group were significantly higher than those in the sham group (P <0.05), but the protein expression level of BDNF decreased in 1 day group and increased in 3 days group (P <0.05). Compared with the HIBD group, the C3, RAGE and TNF-α protein expression levels were significantly attenuated in the HIBD+GAS group (P <0.05), and the protein expression levels of BDNF and IGF-1 further increased(P<0.05). The protein expression of S100A10 in the 3 days group was higher than that in the HIBD group after GAS treatment (P<0.05). The immunohistochemical staining results of C3, S100A10, and RAGE in the 1 day and 3 days groups after HIBD were consistent with Western blotting results. Furthermore, the protein expressions of RAGE and TNF-α were significantly enhanced in OGD-stimulated astrocytes (P<0.05). After GAS intervention, while the expressions of both RAGE and TNF-α decreased significantly (P<0.05), the expressions of BDNF and IGF-1 increased significantly (P<0.05). Conclusion  With inhibiting the up-regulation of RAGE signal in astrocyte after HIBD and expressions of A1 astrocyte and neuroinflammatory factors, gastrodin can promot the expressions of A2 astrocyte and nutritional factors, which play an important role in neuro-protective effect. 

Objective  To explore the neuroprotective effects and mechanisms of the sesquiterpene lactone compound ACT001 on rotenone (ROT) -induced Parkinson’s disease (PD) model mouse.  Methods  SPF C57BL/6 mice were randomly divided into 6 groups, including control group, solvent control group, ROT model group, ACT001 5 mg/kg group（ROT+ACT001-5）, ACT001 20 mg/kg group（ROT+ACT001-20）, and levodopa(L-dopa) positive control group(ROT+L-dopa)，with 9 mice in each group. The control group received an equivalent amount of intraperitoneal injection of saline, the solvent control group received an equivalent amount of rotenone solvent without rotenone, the remaining groups of mice were used to establish a PD mouse model by intraperitoneal injection of rotenone. Mice in different ACT001 dosage groups received intraperitoneal injections of high and low doses of ACT001, while the positive control group received levodopa intraperitoneally for 15 consecutive days. Behavioral changes in mice were assessed using open field, rotarod, pole-climbing, and balance beam tests. Immunofluorescence (IF) assay to detect the expression of tyrosine hydroxylase (TH) neurons，content of TH-positive fibers in the striatum and to detect the activation status of nigrostriatal microglia in the mouse midbrain; Real-time PCR was employed to measure the levels of interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α) in the substantia nigra of the mouse brain. Western blotting was used to measure the protein levels of TH, nuclear factor-κB (NF-κB) p65, NF-κB inhibitor α (IκBα), and phosphorylated IκBα (p-IκBα) in the substantia nigra of the mouse brain.  Results  Compared to the control group and the solvent control group, the rotenone-induced PD model group exhibited motor impairments in behavioral tests, a decrease in the number of TH positive neurons in the substantia nigra (P <0.0001), decreased levels of TH-positive fibers in the striatum, activation of midbrain substantia microglia，and elevated levels of IL-6,  IL-1β, TNF-α, p-IκBα, and NF-κB p65 expression. ACT001 significantly improved the behavioral impairments and substantia nigra damage in PD mice, increased the number of TH-positive neurons in the substantia nigra, increased levels of TH-positive fibers in the striatum, inhibition of microglial cell activation in the midbrain substantia nigra, and elevated the protein expression levels of IκBα while reducing the levels of IL-6, IL-1β, TNFα, -IκBα, and NF-κB p65 in the substantia nigra ( P<0.05). At a dose of 5 mg/kg, ACT001 significantly improved behavioral impairments in rotenone-induced PD mice, reduced the loss of dopaminergic neurons, and its mechanism may be related to the inhibition of the NF-κB  signaling pathway and the suppression of inflammation. In summary, the intervention of ACT001 in the rotenone-induced PD mouse model inhibited the inflammatory response in the midbrain, increased the number of TH-positive neurons, and augmented the population of dopaminergic neurons in the substantia nigra, exerting a protective effect on neurons.   Conclusion  ACT001 significantly improves behavioral deficits in ROT-induced PD mice, ameliorates of dopaminergic neuron loss from the midbrain substantia nigra and striatum, inhibits the activation of nigrostriatal microglia in the midbrain, and suppresses inflammatory responses by inhibiting the activation of the NF-κB signaling pathway. 

Objective To construct a mouse model of alcoholic liver fibrosis and explore the effect of supplementing exogenous thyroid hormone T3 on oxidative stress in liver. Methods  Eighty mice were randomly divided into 6 groups, normal control group, alcoholic liver fibrosis(ALF) model group, and low concentration T3 intervention group (25 μg/kg), medium concentration T3 intervention group (50 μg/kg), high concentration T3 intervention group (100 μg/kg) and T3 control group (the concentration of T3 is 100 μg/kg). A model of mice alcoholic liver fibrosis was established by using alcoholic liquid feed combined with 31.5% ethanol gavage. From the sixth week, mice in the T3 intervention and T3 control group were injected with corresponding concentrations of T3 intraperitoneally for three weeks. Mice in the control and T3 control groups were fed with control liquid feed. The degree of mice liver injury and fibrosis was evaluated through the sirius red staining, Western blotting, and serum biochemical testing. The activity of superoxide dismutase(SOD), the content of glutathione(GSH) and malondialdehyde(MDA) in liver tissue were detected by ELISA, and the protein expressions of microtubule-associated protein light chain 3-Ⅱ(LC3-Ⅱ) and p62 were detected by immunohistochemistry and Western blotting. Results  The liver structure and function in the ALF group were severely damaged, autophagy was inhibited, and the oxidative stress response was significantly enhanced compared with the control group. Compared with the ALF group, the recovery of liver functional and structure and autophagy were showed in the T3 intervention group, and SOD activity and GSH content in the liver increased in the low and medium concentrations of T3 intervention groups, while MDA content significantly decreased. In the high concentration T3 intervention group, it showed the same increase in SOD activity, a significant decrease in MDA content, while the content of GSH was lower than that in the control group, which was not different with the ALF group. Conclusion  Appropriate supplementation of T3 could affect the occurrence and development of alcoholic liver fibrosis by restoring the liver autophagy to inhibit the oxidative stress response. 

Objective To investigate the effect and mechanism of edaravone (Eda) on myocardial injury in chronic heart failure (CHF) rats by regulating Notch/Hes-1 signaling pathway.   Methods The CHF rat model was established and the rats were separated into sham surgery (S) group, model(M) group, low dose Eda (Eda-L) group, medium dose Eda (Eda-M) group, high dose Eda (Eda-H) group, and Eda-H + Notch signal pathway inhibitor DAPT (Eda-H + DAPT) group, with 25 rats in each group. Echocardiography was applied to detect the levels of left ventricular end diastolic diameter (LVEDd), left ventricular end-systolic diameter (LVEDs), and left ventricular ejection fraction (LVEF) in rats. ELISA was applied to detect levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, malondialdehyde (MDA), superoxide dismutase (SOD), and angiotensin Ⅱ (Ang Ⅱ) in serum. Myocardial infarction was observed by 2,3,5-triphenyl tetrazolium chloride(TTC) staining. HE staining, TUNEL staining and Masson staining were applied to observe the morphological changes of myocardial tissue, myocardial cell apoptosis and myocardial fibrosis respectively. immunohistochemistry was applied to detect the expression of collagen Ⅰ and angiotensin converting enzyme 2 (ACE2) proteins in myocardial tissue. Western blotting was applied to detect the expression of Notch 1, Hes-1, transforming growth factor-β1 (TGF-β1), Bcl-2, Bax, and Caspase-3 proteins in myocardial tissue.   Results Compared with the sham group, the distribution of cardiomyocytes in model group was disordered, and severe inflammatory symptoms. There was a large amount of blue collagen deposition between the perivascular area and the myocardium. The LVEDd, LVEDs, TNF-α, IL-1β, IL-6, MDA and Ang Ⅱ levels, myocardial infarction size, cardiomyocyte apoptosis rate, Collagen Ⅰ, Bax, Caspase-3 and TGF-β1 protein expressions increased obviously (P<0.05), the LVEF, SOD levels, ACE2, Bcl-2, Notch 1, and Hes-1 protein expressions were obviously reduced (P<0.05). Compared with the model group, the myocardial tissue damage was reduced in the Eda-L, Eda-M, and Eda-H groups, with reduced inflammatory cell infiltration and collagen deposition; The LVEDd, LVEDs, TNF-α, IL-1β, IL-6, MDA and Ang Ⅱ levels, myocardial infarction size, cardiomyocyte apoptosis rate, collagen Ⅰ, Bax, Caspase-3 and TG-β1 protein expressions reduced obviously(P<0.05), the LVEF, SOD levels, ACE2, Bcl-2, Notch 1, and Hes-1 protein expressions increased obviously (P<0.05). Notch signaling pathway inhibitor DAPT reversed the protective effect of edaravone on myocardial injury in rats with CHF (P<0.05).   Conclusion Edaravone may improve myocardial injury in CHF rats by activating Notch/Hes- 1 signaling pathway.

Objective To reveal the development characteristics of fat percentage and muscle mass in three nomadic populations in the Hexi Corridor of Gansu.   Methods Bioelectrical impedance analysis was used to determine the values of 13 indexes of fat percentage and muscle mass in 263 cases of Gansu Kazakhs, 400 cases of Gansu Mongols, and 362 cases of Yugu adults.     Results In the three nomadic populations of the Hexi Corridor, visceral fat level of males was significantly positively correlated with age, while total body muscle mass and estimated bone mass were significantly negatively correlated with age. In females, percent body fat, visceral fat grade, percent left and right upper limb fat, percent right lower limb fat and percent trunk fat were all significantly positively correlated with age, while trunk muscle mass was significantly negatively correlated with age. The result  of principal component analysis showed that the three nomadic populations in the Hexi Corridor were close to each other in terms of fat percentage and muscle mass characteristics, with high visceral fat grades in males and normal visceral fat grade in females. Among the 13 populations, three nomadic groups in the Hexi Corridor had high fat percentage and muscle mass. Overall, the nomadic population had greater fat percentage and muscle mass than the semi-agricultural and semi-pastoral population, and even more significantly greater than the agrarian population. The long-term integration of the historical Hexi Corridor populations result ed in the relative proximity of the genetic structure of three nomadic populations, which was a genetic factor for the proximity of their fat percentage and muscle mass. Higher per capita disposable income was a socio-economic factor for high fat percentage and muscle mass among Gansu Kazakhs and Gansu Mongolians. Low average annual temperature was an environmental factor for high muscle mass among Gansu Kazakhs and Yugus.    Conclusion Gansu Kazakhs, Gansu Mongols, and Yugus have the fat percentage and muscle mass characteristic of northern Chinese populations.

 Objective To investigate the effects of microRNA (miR)-145 delivered by exosomes (Exo) on platelet activation and vascular endothelial function in rats with coronary atherosclerotic heart disease (CAHD).  Methods   HEK239 cells were transfected with miR-negative control(NC) and miR-145, and the transfection effect was detected by Realtime PCR. Exo was isolated from HEK239 cells transfected with miRNA-NC and miR-145. The morphology and size distribution were observed by transmission electron microscopy. The expressions of CD81, heat shock protein 70（HSP70）and tumor susceptibility gene 101（TSG101）were detected by Western blotting. The experiment included control group, model group, miR-NC Exo group and miR-145 Exo group, with 8 rats in each group. After treatment, the ejection fraction (EF), fractional shortening rate (FS), left ventricular enddiastolic diameter (LVIDD) and left ventricular end-systolic diameter (LVIDS) of rats were determined by ultrasonic diagnostic instrument. HE staining was performed to observe the pathological changes of myocardial tissue and aortic tissue, and ELISA was used to determine serum platelet activating factor (PAF), β-platelet globulin (β-TG), platelet membrane glycoprotein Ⅱa/Ⅲb (GPⅡa/Ⅲb), nitric oxide (NO), endothelin-1 (ET-1) and vascular endothelial growth factor (VEGF). Immunohistochemical staining was used to detect the expression of endothelial nitric oxide synthase (eNOS) in aorta tissue.  Results  The relative expression level of miR-145 in HEK239 cells transfected with miR-145 was significantly higher than that in untransfected and transfected miR-NC cells (P <0.05). The isolated particles showed typical cup-shaped or disk-shaped vesicles, most of which were distributed at 100 nm in diameter. CD81, HSP70 and TSG101 proteins were highly expressed, and the relative expression level of miR-145 in Exo transfected with miR-NC was significantly lower than that in Exo transfected with miR-145 (P <0.05). Compared with the miR-NC Exo group, EF and FS of miR-145 Exo group increased significantly(P <0.05), while LVIDD and LVIDS decreased significantly(P <0.05), and the pathological changes of myocardial tissue and aortic tissue were better improved. The contents of PAF, β-TG, GPⅡa/Ⅲb, ET-1 and VEGF in serum were further significantly decreased (P <0.05), while the content of NO was also significantly increased (P <0.05), and the positive expression rate of eNOS in aortic tissue was further significantly increased (P <0.05).  Conclusion  MiR-145 delivered by Exo could inhibit platelet activation and improve vascular endothelial function in coronary heart disease model rats, and plays a protective role in coronary heart disease model rats. 

Objective  To establish a normal three-dimensional model of the hip bone in adolescents aged 10-19 years old, analyze the morphology and positional parameters of the posterior superior iliac spine of the hip bone among different genders, sides, and ages, which can supplement the study of the anatomical morphology of the hip bone and to provide a reference for the diagnosis of the clinically relevant diseases and for the therapeutic manipulation and localization of the hip bone.  Methods  Forty adolescent patients aged 10-19 years without previous spinal pelvic diseases were selected, and the pelvic CT image data were collected and imported into Mimics 21.0 software to establish the model. The relative position parameters of the posterior superior iliac spine and the surrounding anatomical landmarks included the length from the posterior superior iliac spine to the anterior superior iliac spine (ab), the length from the tip of the posterior superior iliac spine to the sciatica (ac), the length from the tip of the posterior superior iliac spine to the pubic tubercle (ae), the length from the tip of the posterior superior iliac spine to the midpoint of the posterior margin of the auricular joint surfaces (af), the length from the tip of the posterior superior iliac spine to the iliac spine turn (ag), and the length from the sciatica tubercle to the highest point of the iliac spine (cd). The local parameters of the posterior superior iliac spine included the width (W0) and the thickness (H0) at point A. The maximum width of the posterior iliac spine (WMAX), its distance from point a (D0), and the width of the iliac spine were measured at 0.5, 1, and 1.5 cm from point a, and were recorded sequentially as W1, W2, and W3. The width of the iliac spine at the turn of the iliac spine (point g) was measured (W4). The relative positions and parameters of the posterior superior iliac spine to the surrounding anatomical landmarks and the localized parameters of the posterior superior iliac spine were compared sequentially for different genders, sides, and age groups.  Results  In the measurement result  of the parameters of the posterior superior iliac spine and the surrounding anatomical landmarks, the differences in the comparisons between different genders of the ac, ae, and af indexes were statistically significant (P<0.05), and the differences in the comparisons between different genders of the ab, ag, and cd indexes were not statistically significant (P >0.05). The differences in the comparisons between the right and left sides of the ab, ac, ae, af, ag, and cd indexes were not statistically significant (P>0.05). The difference in comparison between different age groups of ab, ac, ae, af, ag, and cd indicators was statistically significant (P<0.05). In the measurement result  of the local parameters of the posterior superior iliac spine, the difference in the comparison between the sexes of the W0, W1, W2, WMAX, and H0 indexes was statistically significant (P<0.05), and the difference in the comparison between the sexes of the W3, W4, and D0 indexes was not statistically significant (P>0.05); And the difference in the comparison between the left and right sides of the W0, W1, W2, and the right and left sides of the W3, W4, WMAX, D0, and H0 indexes was not statistically significant (P>0.05); The difference between W0, W1, W2,W3, W4, WMAX, D0, H0 indicators compared between different age groups was not statistically significant (P>0.05). Conclusion  Adolescent females have overall greater pelvic parameters than males, with wider and thicker tips of the posterior superior iliac spine in females and narrower and thinner tips of the posterior superior iliac spine in males; Pelvic parameters show a tendency to increase with age, while the width and thickness of the posterior superior iliac spine, as well as the width of the cephalic end to the iliac spine remain essentially unchanged.

Objective  To explore the mechanism of inhibiting a disintegrin and metalloprotease 8 (ADAM8) expression on inflammatory damage in alcoholic liver fibrosis mice. Methods  C57BL/6N male mice were randomly divided into the control group, the alcohol group, and the plasmid group, with 10 mice in each group. The alcohol group and plasmid group were fed alcohol liquid feed on a daily basis and gavaged with 31.5% ethanol (5g/kg, twice a week); The control group was fed control liquid feed and gavaged with an equal amount of saline. The plasmid group was injected with the effective plasmid ADAM8-small guide RNA3(sgRNA3)(2g/kg, twice a week) to inhibit the ADAM8 gene through the tail vein, while the alcohol group was injected with an equal amount of saline through the tail vein for 8 weeks to induce alcoholic liver fibrosis. After eyeball blood collection, the mice were euthanized，and their liver was separated and extracted. Sirius red and HE staining were employed to assess liver fibrosis and damage; Western blotting was used to determine the expression of α-smooth muscle actin(α-SMA), collagenⅠ, and ADAM8; Real-time PCR was used to measure the expression of ADAM8 mRNA; the expression of ADAM8, transforming growth factor-β1(TGF-β1), p-p38 MAPK and heat shock protein 27(HSP27) proteins was detected by Western blotting, Biochemical detection were used to detect alanine aminotransferase(ALT) and aspartate transaminase(AST) activity; tumor necrosis factor-α(TNF-α) and interleukin-1(IL-1) levels were determined by ELISA. Results  The alcohol group had increased collagen fiber volume fraction, liver injury scores, and positive area rates of α-SMA and collagenⅠ; the expression of ADAM8 mRNA and ADAM8 protein increased, with increased positive area rate; and levels of AST, ALT, TNF-α, and IL-1 were higher, along with increased expression of TGF-β1, p-p38MAPK, and HSP27 proteins. In the plasmid group, the collagen fiber volume fraction, liver injury scores, and positive area rates of α-SMA and collagenⅠ was reduced; the expression of ADAM8 mRNA and protein was reduced, with decreased positive area rate, and levels of AST, ALT, TNF-α, and IL-1 were lower, along with reduced expression of TGF-β1, p-p38MAPK, and HSP27 proteins.  Conclusion  Downregulation of ADAM8 expression can alleviate inflammatory damage by inhibiting TGF-β1/p38MAPK signaling pathway to improve alcoholic liver fibrosis in mice. 

Objective  To explore the commonalities and differences of the body characteristics of different language groups in China.  Methods  The body index data of 65 343 adults (29 667 males and 35 676 females) from 8 language groups in China were measured. Principal component analysis was used to explore the characteristics of human body development in China. Results  Among the eight language groups in China, the three ethnic groups of the Altai languages have the largest body weight, large trunk circumference, high stature, long lower limbs, and long trunk. The body height, length, weight and trunk circumference of the Han ethnic group were slightly inferior to those of the Altaic ethnic group. The Tibetan-Burmese ethnic group belongs to the group with higher body height, length, weight and trunk circumference in the southern ethnic group. In contrast, the Zhuang-Dong ethnic group, the Miao-Yao ethnic group and the South Asian ethnic group in the south had smaller trunk circumference, lighter weight, shorter stature, shorter lower limbs and shorter trunk.  Conclusion  The body characteristics of the northern (or southern) language groups are relatively close, which reflects the commonality of the characteristics of the Chinese language groups. The differences in the characteristics of Chinese language groups are mainly reflected in the fact that the index values of the three language groups in the north are significantly larger than those of the four language groups in the south. Genetic factors, geographical environment factors and social development factors all affect the body characteristics of Chinese language ethnic group. 

With the rapid development of the Internet, the problem of internet gaming disorder (IGD) among adolescents has gradually become prominent. IGD has caused serious harm to their physical and mental health, and it is difficult to withdraw and treat. In 2019, the World Health Organization (WHO) officially listed Gaming Disorder (GD) in the diagnostic category and included it in the 11th edition of the International Classification of Diseases. In China, the number of adolescent internet users has approached 200 million, and the number of IGD patients is relatively large. It is urgent to make breakthroughs in the cognition and treatment of IGD. Domestic and foreign studies have shown that IGD’s physical and psychological harm to adolescents is related to the abnormal activation and functional connection damage of structures such as the prefrontal lobe, limbic system, and striatum, which in turn causes neurocognitive disorders, executive dysfunction, difficulty in emotional regulation, abnormal reward and punishment feedback, behavioral abnormalities and other functional disorders; therefore, this article aims to systematically review the research literature on IGD in recent years, and use neurophysiological imaging research method  to sort out the changes in the brain structure and function of adolescents with IGD, in order to improve the understanding of the pathophysiology of the disease, and assist in further clinical diagnosis, treatment, application and research design. 

Objective  To investigate the association of digit ratio with single nucleotide polymorphism (SNP) at three loci (rs17576, rs3918249, rs9509) of matrix metallopeptidase 9 (MMP-9) gene.   Methods  A total of 804 Ningxia Han youths (399 males and 405 females) were used as the study subjects. A digital camera was used to take frontal photographs of the hands, and image analysis software was used to mark the anatomical points and measure the lengths of each finger of both hands (2D, 3D, 4D, 5D); Multiplexed PCR was used to detect the three polymorphic sites of the MMP-9 gene, SPSS 25.0 and R Studio software were used for data analysis and plotting.   Results  The 2D/3D (P<0.05) and 2D/4D (left,  P<0.01, right,  P<0.05) of both hands, 2D/5D (P<0.01), 3D/5D, 4D/5D (P<0.05) of the right hand, and 3D/4D (P<0.05) of the left hand in female youths of Ningxia Han were significantly higher than those in males, Differences in genotypes and allele frequencies at all 3 loci of the MMP-9 gene were not statistically significant between genders (P>0.05). Right hand 2D/4D was significantly associated with genotypes at the rs17576 and rs3918249 loci in male youths (P<0.05).    Conclusion  MMP-9 gene SNPs (rs17576 and rs3918249) may be associated with the formation of 2D/4D of Ningxia Han male youths. 

Objective  To measure the distance between the lateral compression Ⅱ (LC-Ⅱ) screw guide needle and the surrounding important structures around the anterior inferior iliac spine in pelvic fractures and to locate the needle point, so as to provide anatomical reference for clinical nail placement. Methods  Totally 40 adult gross specimens of embalming were implanted with LC-Ⅱ screw guide needle under the surveillance of C-arm machine, and the specimens were dissected. The shortest distance between the insertion point and the lateral femoral cutaneous nerve, femoral nerve, femoral artery, femoral vein, anterior superior iliac spine and inguinal ligament was measured. The triangle was constructed between the insertion point, anterior superior iliac spine and inguinal ligament, and the exact location of the entry point was calculated. Results  The average distance between the insertion point of the male needle and the femoral vein was（50.67±7.29）mm> the anterior superior iliac spine (43.83±7.58) mm> the femoral artery (38.35±6.63) mm> the femoral nerve (31.17±1.67) mm= the inguinal ligament (28.69±6.59) mm> the lateral femoral cutaneous nerve (7.98±3.81) mm. The mean distance between the insertion point of the female needle and the anterior superior iliac spine was (45.28±7.07) mm= femoral vein (43.72±6.89) mm> femoral artery (33.76±6.33) mm> femoral nerve (25.66±6.46) mm= inguinal ligament (23.22±5.00) mm> lateral femoral cutaneous nerve (8.97±4.76) mm. The projection distance of the entry point was 31.77mm for men and 38.41mm for women. The Angle b was 42.81°for men and 31.71°for women. Conclusion  The lateral femoral cutaneous nerve is most vulnerable to injury when LC-Ⅱ screw is inserted, and the risk of injury has nothing to do with sex. The insertion point positioning method  a and b made LC-Ⅱ screw placement quickly, safely and accurately, and reduced fluoroscopy time and frequency. 

Objective  To investigate the effects of inhibition of chemokine C-X-C motif receptor 7(CXCR7) expression on the proliferation, migration, differentiation and mitochondrial function of human urine-derived stem cells(USCs) under hypoxia.  Methods  CXCR7 expression was inhibited by siCXCR7 and detected by Real-time PCR and Western blotting in hypoxia group treated with 3%O2 for 48 hours. Cell proliferation was detected by clonal formation assay and cell growth curve. Cell migration ability was detected by scratch assay and Transwell assay. Alkaline phosphatase, alizarin red, oil red O and alcian blue staining were used to detect the multidirectional differentiation ability of cells. Mitochondrial function was evaluated by JC-1 fluorescent probe, adenosine triphosphate(ATP) and reactive oxygen species(ROS). Results  Compared with the normal oxygen group, the expression of CXCR7 in USCs in hypoxia group was significantly up-regulated, and hypoxia promoted the proliferation, migration and clonogenesis of USCs. SiCXCR7 inhibited the expression of CXCR7 and inhibited the effects of hypoxia on the proliferation, migration and clonogenesis of USCs, but had no effect on cell differentiation. Hypoxia treatment increased mitochondrial membrane potential and ATP levels, and decreased the production of reactive oxygen species, while CXCR7 inhibition decreased mitochondrial membrane potential and ATP production. Conclusion  Hypoxia may enhance mitochondrial function of USCs through the CXCR7 signaling pathway, thereby promoting cell proliferation and migration.

Objective  To investigate the mechanism of neuronal apoptosis induced by cyclooxygenase-2 (COX-2) after cerebral ischemia/reperfusion（CI/R）injury in rats.  Methods  Totally 45 male SD rats were divided into 3 groups by random number method, sham operation group (sham), model group (CI/R), COX-2 inhibitor group (NS-398). Blocking the middle cerebral artery to create a model, at the beginning of ischemia, NS-398 group was intraperitoneally injected with NS-398（20 mg/kg）, while sham group and CI/R group were injected with the same amount of DMSO. Rats were performed for neurofunctional scores after 2 hours ischemia. After 24 hours reperfusion, 2,3,5-triphenyltetrazolium chloride (TTC) staining was used to detect the infarct volume of rats. Meanwhile, cerebral tissue from penumbra area of frontal parietal cortex on ischemic side was taken, Nissl staining and TUNEL method were used to detect neuronal damage and apoptosis respectively, and finally Western blotting was used to detect the expression levels of COX-2,Bcl-2 and Bax proteins.  Results  The neurofunctional scores of rats, cerebral infarction volume, apoptosis index, the expressions of COX-2 and Bax in CI/R group were higher than those in the sham group (P<0.05)，the expression level of Bcl-2 and the number of neurons were lower than those in the sham group (P <0.05); The neurofunctional scores of rats, cerebral infarction volume, apoptosis index, the expression levels of COX-2 and Bax in NS-398 group were lower than those in CI/R group (P<0.05), the expression level of Bcl-2 and the number of neurons were higher than those in CI/R group (P<0.05).  Conclusion  COX-2 may promote neuronal apoptosis after cerebral ischemia/reperfusion injury by regulating the expressions of Bcl-2 and Bax. 

Objective  To explore the anatomical landmarks and segmentation method  for the intraoperative identification of the cervical segment of the internal carotid artery by studying cadaveric dissections with an endoscopic transoral medial pterygomandibular fold approach and to investigate its clinical significance.   Methods  The head specimens of five fresh frozen cadavers were dissected in the anatomical laboratory of the Surgical Treatment Technology Innovation Unit of Nasal Skull Base Tumor in Eye & ENT Hospital of Fudan University. The parapharyngeal space was dissected layer by layer through the endoscopic transoral medial pterygomandibular fold approach, and the location marks of parapharyngeal internal carotid artery (ppICA) and adjacent structures of ppICA were anatomically studied. The anatomical landmarks associated with ppICA were observed and characterized, and the ppICA was segmented anatomically according to its adjacent structures. Then, the length of each ppICA segment was measured.  Results  Muscle structures were essential anatomical landmarks for an endoscopic transoral pterygoid medial approach that identifies mandibular folds. The first layer of muscles included the superior pharyngeal constrictor, tensor veli palatini, and medial pterygoid muscles. The second layer includes the stylopharyngeus, styloglossus, longus capitis, and levator veli palatini muscles. The stylopharyngeal and levator veli palatini muscles were close to the ppICA and were reliable landmarks for locating the ppICA. Furthermore, the ppICA was divided into three segments according to their positional relationship with the ppICA. The first segment of ppICA(P1ICA) was located between the greater horn plane of the hyoid bone and the intersection plane between the upper margin of stylopharyngeal muscle and ppICA. The second segment of ppICA (P2ICA) was between the plane where the upper edge of the stylopharyngeal muscle intersected with the ppICA and the plane where the projection of inferior edge of the levator veli palatini muscle intersected with the ppICA. The third segment of ppICA (P3ICA) was between the intersection of the lower margin projection of the levator veli palatini muscle and ppICA and the external orifice of the carotid canal. The P2ICA was within an anatomical region bounded by the levator veli palatini muscle, longus capitis muscle, and stylopharyngeus muscle. This region was termed “ICA window” in this paper measured under the cadaver head specimen, the lengths of P1ICA, P2ICA, and P3ICA were (36.5±7.3) mm, (15.5±1.6) mm, (7.4±1.7) mm respectively.   Conclusion  The muscular structure refers to the relatively constant anatomical reference landmarks within the endoscopic transoral medial pterygomandibular fold. The stylopharyngeus and levator veli palatini muscles are reliable landmarks for precisely locating and segmenting the ppICA, thus having essential clinical implications.  

Objective To explore the pathogenesis of Alzheimer’s disease by examining the effects of dihydroartemisinin(DHA) on cognitive behavior, hippocampal, cerebral cortex and retinal cell morphology, β-amyloid(Aβ) and autophagy-related proteins in 5×FAD mice.   Methods  Twenty 5×FAD mice and 5 wild type (WT) mice were selected, all of which were female. The 5×FAD mice were randomly divided into model (M) group, donepezil (D) group, low-dose DHA (DHA-L) group, and high-dose DHA (DHA-H) group. The WT and M groups were not treated, and the D group was given donepezil 0.1 mg/kg per day. DHA-L group and DHA-H group were given 10 mg/kg and 20 mg/kg DHA per day, respectively. Group D, group DHA-L and group DHA-H were given intragastric administration once a day for 3 months. The changes of in cognitive behavior were measured by Morris experiment. HE staining was used to observe the arrangement and morphology of nerve cells in cerebral cortex, hippocampus and retina. The expressions of Aβ protein in cerebral cortex, hippocampus and retina were detected by immunohistochemistry. Western blotting detected the expression of autophagy related proteins (LC3-Ⅰ, LC3-Ⅱ, Beclin-1, P62, β-actin).   Results  The DHA-H group and the D group exhibited more frequent adoption of both linear and trending exploration routes. Compared to the model group, significant differences in the contents of Aβ  in the hippocampal CA1, cerebral cortex S1, and retinal were observed (P<0.0001) in the other four groups. The analysis also showed significant differences in autophagy-associated proteins between the DHA-L,  DHA-H, and model groups (P<0.01).  Conclusion  DHA improves cognitive function and increases the number of nerve cells in mice. It also reduces Aβ content in the cerebral cortex, hippocampus, and retina, along with improving autophagy-associated protein deposition in mice.  

Objective  On the basis of preliminary evidence that microRNA(miR)-181b-5p inhibits osteogenic differentiation of human bone marrow mesenchymal stem cells (BMMSCs), the regulatory mechanism was further explored. Methods  Isolation, culture and identification of BMMSCs from the bone marrow of five healthy adults. The targeting relationship between miR-181b-5p and Sprouty 4(SPRY4) was investigated by bioinformatics software prediction, double luciferase reporter gene detection, Real-time PCR and Western blotting experiments. BMMSCs were divided into three groups, miR-181b-5p overexpression negative control group; miR-181b-5p overexpression group; miR-181b-5p overexpression +SPRY4 silenced group. Alkaline phosphatase(ALP) staining and ALP activity analysis were used to determine the effect of early osteogenic differentiation. The precipitation of calcium nodules was detected by alizarin red staining. The mRNA and protein expression levels of osteogenic differentiation marker genes were detected by Real-time PCR and Western blotting.  Results  BMMSCs were successfully isolated and identified. MiR-181b-5p specifically binds to the 3’UTR of SPRY4 mRNA. After overexpression of miR-181b-5p, the expression of SPRY4 protein level was significantly down-regulated, but there was no significant change in mRNA level. Knocking down the target gene SPRY4 blocked the effect of miR-181b-5p inhibitors on promoting osteogenic differentiation of cells. Conclusion  MiR-181b-5p inhibits osteogenic differentiation of BMMSCs by downregulating SPRY4 protein.